We have previously shown that anti-Ig heavy chain-specific antibodies, when injected into mice from birth onward, can achieve severe multiclass or class-specific immunosuppression of normal B cells. We have also shown that these antibodies, first administered at birth or in adulthood, can prevent the growth of certain murine malignant lymphoid cells, particularly those of plasmacytomas. We have recently established the Fc dependence of such suppresson for normal B cells and used this observation to base a working model for the mode of action involved. Our study of heavy chain isotype suppression will continue for the dual purposes of refining our model which explains the mechanism of this phenomenon and of developing applied models for the study of several disease processes of great clinical significance. Refinements of the mechanistic model will center around determination of: (1)\the manner in which surface Ig binding and Fc attachment by anti-Ig interact to generate a direct inhibitory immune signal (by studying the blocking capacity of F(ab')2 fragments); (2)\the possible participation of suppressor cells (by adoptively transferring cells from suppressed mice); (3)\the role of lymphocyte surface IgD (by using antidelta antibodies); (4)\the nature of surface determinants of suppressed cells (by flow cytometry); and (5)\the nature of lymphoid changes accompanying adultinitiated anti-Ig treatment (by morphological and histological examination). The focus of applied model development will now be narrowed from the three previous cases of helminth expulsion, IgE suppression and malignant lymphoid cell inhibition to a concentrated effort on plasmacytoma control.